Clostridial Diseases of Horses: A Review

Abstract

The clostridial diseases of horses can be divided into three major groups: enteric/enterotoxic, histotoxic, and neurotoxic. The main enteric/enterotoxic diseases include those produced by Clostridium perfringens type C and Clostridioides difficile, both of which are characterized by enterocolitis. The main histotoxic diseases are gas gangrene, Tyzzer disease, and infectious necrotic hepatitis. Gas gangrene is produced by one or more of the following microorganisms: C. perfringens type A, Clostridium septicum, Paeniclostridium sordellii, and Clostridium novyi type A, and it is characterized by necrotizing cellulitis and/or myositis. Tyzzer disease is produced by Clostridium piliforme and is mainly characterized by multifocal necrotizing hepatitis. Infectious necrotic hepatitis is produced by Clostridium novyi type B and is characterized by focal necrotizing hepatitis. The main neurotoxic clostridial diseases are tetanus and botulism, which are produced by Clostridium tetani and Clostridium botulinum, respectively. Tetanus is characterized by spastic paralysis and botulism by flaccid paralysis. Neither disease present with specific gross or microscopic lesions. The pathogenesis of clostridial diseases involves the production of toxins. Confirming a diagnosis of some of the clostridial diseases of horses is sometimes difficult, mainly because some agents can be present in tissues of normal animals. This paper reviews the main clostridial diseases of horses.

Clostridioides (Clostridium) difficile–associated disease, epiploic foramen entrapment, and gastric rupture in a Thoroughbred racehorse: case report and literature review

“…C. difficile TcdA/TcdB were detected in small intestinal contents, which confirms a diagnosis of CDAD, 8,20 and C. difficile was isolated from small intestine, colon, and cecum (Table 1). Isolation of C. difficile is not confirmatory, given that a small percentage of healthy horses may carry the organism 6,9 ; however, in our case, bacterial isolation in 3 different intestinal segments further supports a diagnosis of CDAD given that the toxins were also detected.…”

“…21 CDAD in adult horses has a longer clinical course than in foals. 20 In our case, the neutrophilic aggregates and fibrin thrombi detected in the lamina propria of the segments of small intestine not involved in the herniation were likely related to CDAD. 8 The microscopic lesions observed in the wall of the incarcerated segment seemed very acute, with a predominance of hemorrhage and necrosis without remarkable neutrophilic tissue infiltrates, hemosiderosis, or fibrosis.…”

“…9 C. difficile –associated disease (CDAD) in adult horses usually has a more protracted clinical course than in foals, and clinical signs include abdominal pain, fever, and diarrhea. 9,20 Antibiotic administration and hospitalization may predispose horses to develop CDAD, but other, non-defined risk factors could play a role. 8,25 On autopsy, there may be watery and hemorrhagic-to-green intestinal contents and pseudomembrane formation; adult horses usually have a more aboral distribution of the lesions, with the cecum and colon most often affected, although lesions in the small intestine can also occur.…”

“…Nevertheless, given that a solid diagnosis of another known cause of enterocolitis in horses (CDAD) was made, the role of P. sordellii was probably secondary; exclusion of other agents has been proposed among the diagnostic criteria for P. sordellii –associated enterocolitis in horses. 15,20 In addition, large numbers of Escherichia coli and mixed flora were isolated from the abdominal cavity and were considered possible contributors to peritonitis further to release of gastric content to the abdominal cavity. As well, no bacteria were isolated from the lung, no parasite eggs or oocysts were detected by fecal flotation, and the hepatic heavy metal and selenium concentrations were within acceptable or nondiagnostic ranges for horses.…”

“…Diagnosis is confirmed by the detection of TcdA and TcdB in intestinal contents by ELISA. 8,20 Here we describe the results of the postmortem examination of a horse that had concurrent CDAD, EFE, and gastric rupture. We discuss the possible sequence of events and pathogenesis, and review some of the available literature about these conditions in horses.…”